Cytokines, Monoamines and Behavior

Reply to Grover, symposium 615, TNF-alpha

Shawn Hayley

In reply to Grover: Thanks for your posting. Yes I am enjoying the conference, I think the internet provides an excellent forum for scientific meetings. TNF-a has multiple sites of action and it is likely that it’s ip administration resulted in the activation of receptors in the gut, liver, spleen (among others) and possibly the brain. A limited amount of systemically administered TNF-a can reach the brain through a saturable transport mechanism. However, it is also possible that  de novo synthesis of TNF-a was induced in the brain or that a secondary mediator, such as prostaglandin E2 may be responsible to some of the cytokine’s effects.  A similar time course (progressive increase with the passage of time) for the sensitization of sickness behavioral alterations and plasma corticosterone release led us to believe that a similar mechanism may be responsible for these effects. However, an earlier sensitization effect observed for noradrenergic activity within the prefrontal cortex suggests a different mechanism may be operative in this respect.


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